Alessia Di Costanzo1, Laura D'Erasmo2, Licia Polimeni2, Francesco Baratta3, Paola Coletta2, Michele Di Martino4, Lorenzo Loffredo2, Ludovica Perri2, Fabrizio Ceci5, Anna Montali2, Gabriella Girelli6, Bruna De Masi6, Antonio Angeloni7, Carlo Catalano4, Marianna Maranghi2, Maria Del Ben2, Francesco Angelico8, Marcello Arca2. 1. Departments of Internal Medicine and Medical Specialties, "La Sapienza" University, Policlinico Umberto I Hospital, Rome, Italy. Electronic address: alessia.dicostanzo@uniroma1.it. 2. Departments of Internal Medicine and Medical Specialties, "La Sapienza" University, Policlinico Umberto I Hospital, Rome, Italy. 3. Departments of Internal Medicine and Medical Specialties, "La Sapienza" University, Policlinico Umberto I Hospital, Rome, Italy; Department of Anatomical, Histological, Forensic Medicine and Orthopedics, "La Sapienza" University, Policlinico Umberto I Hospital, Rome, Italy. 4. Radiological Sciences Department, "La Sapienza" University, Policlinico Umberto I Hospital, Rome, Italy. 5. Department of Cellular Biotechnologies and Hematology, "La Sapienza" University, Policlinico Umberto I Hospital, Rome, Italy. 6. Immunohematology and Transfusion Medicine Unit, "La Sapienza" University, Policlinico Umberto I Hospital, Rome, Italy. 7. Department of Molecular Medicine, "La Sapienza" University, Policlinico Umberto I Hospital, Rome, Italy. 8. Department of Public Health and Infectious Disease, "La Sapienza" University, Policlinico Umberto I Hospital, Rome, Italy.
Abstract
BACKGROUND AND AIMS: Non-alcoholic fatty liver disease (NAFLD) is frequently associated with atherosclerosis. However, it is unclear whether this association is related to excess fat liver storage per se or to metabolic abnormalities that typically accompany NAFLD. To investigate this, we compared individuals with hepatic steatosis driven by metabolic disturbances to those with hepatic steatosis associated with the rs738409 GG genotype in the patatin-like phospholipase domain-containing 3 gene (PNPLA3). METHODS: Carotid intima-media thickness (CIMT), as a surrogate marker of subclinical atherosclerosis, was measured in 83 blood donors with the mutant GG genotype (group G), 100 patients with features of metabolic syndrome (MetS) but the wildtype CC genotype (group M), and 74 blood donors with the wildtype CC genotype (controls). Fatty liver was evaluated by ultrasonography and hepatic fat fraction (HFF) was measured using magnetic resonance (MRS/MRI) in 157 subjects. RESULTS: Compared with group G and controls, group M subjects were older and had increased adiposity indices, dyslipidemia, insulin resistance and elevated transaminase levels (all p < 0.05). They also had a more fatty liver on both ultrasonography and MRS/MRI. After adjustment for confounders (including severity of hepatic steatosis), the median CIMT in group M (0.84 [0.70-0.95] mm) was significantly greater than that in group G (0.66 [0.55-0.74] mm; p < 0.001), which was similar to that in controls (0.70 [0.64-0.81] mm). Results were similar in the subgroup evaluated using MRS/MRI. CONCLUSIONS: Excess liver fat accumulation appeared to increase the burden of subclinical atherosclerosis only when it is associated with metabolic abnormalities.
BACKGROUND AND AIMS: Non-alcoholic fatty liver disease (NAFLD) is frequently associated with atherosclerosis. However, it is unclear whether this association is related to excess fat liver storage per se or to metabolic abnormalities that typically accompany NAFLD. To investigate this, we compared individuals with hepatic steatosis driven by metabolic disturbances to those with hepatic steatosis associated with the rs738409 GG genotype in the patatin-like phospholipase domain-containing 3 gene (PNPLA3). METHODS: Carotid intima-media thickness (CIMT), as a surrogate marker of subclinical atherosclerosis, was measured in 83 blood donors with the mutant GG genotype (group G), 100 patients with features of metabolic syndrome (MetS) but the wildtype CC genotype (group M), and 74 blood donors with the wildtype CC genotype (controls). Fatty liver was evaluated by ultrasonography and hepatic fat fraction (HFF) was measured using magnetic resonance (MRS/MRI) in 157 subjects. RESULTS: Compared with group G and controls, group M subjects were older and had increased adiposity indices, dyslipidemia, insulin resistance and elevated transaminase levels (all p < 0.05). They also had a more fatty liver on both ultrasonography and MRS/MRI. After adjustment for confounders (including severity of hepatic steatosis), the median CIMT in group M (0.84 [0.70-0.95] mm) was significantly greater than that in group G (0.66 [0.55-0.74] mm; p < 0.001), which was similar to that in controls (0.70 [0.64-0.81] mm). Results were similar in the subgroup evaluated using MRS/MRI. CONCLUSIONS: Excess liver fat accumulation appeared to increase the burden of subclinical atherosclerosis only when it is associated with metabolic abnormalities.
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